The present study suggests that the 5-HTT genotype may be a factor that contributes to maintenance of CFS.
This is interesting timing. Darden is about to do a blog on serotonin and fibromyalgia and will relate how increasing her serotonin levels helped her. Mady Hornig recently reported preliminary findings of low serotonin in the guts of people with ME/CFS. Now this study suggests that ME/CFS patients with variants of serotonin transporter genes which reduce the transcription rate of serotonin transporter gene are worse off. The young ME/CFS patients with the gene had fewer steps per day than those without it.
The result is reduced serotonin uptake and increased serotonin levels in the synapses of the nerves. Serotonin has historically been associated with mood disorders but recent research indicates it impacts many areas of the body. We'll see in Darden's blog that serotonin has many immune effects. In fact, without adequate serotonin levels your immune system will not fight off an infection.
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[/fright]The authors suggested that the gene variant - found in about 25% of patients - could contribute to the sympathetic nervous system problems as well. Because roughly equal percentages of ME/CFS patients and healthy controls (21%) carried the suspect gene they don't believe the gene variant makes one more susceptible to getting ME/CFS but that if you have it you're more likely to be worse off.
The Mady Hornig and Ian Lipkin microbiome results are getting more interesting all the time. They believe that the substance serotonin is produced out of - tryptophan - may be being metabolized to kynurenine metabolites instead of serotonin. The kynurenine pathway has been associated with many neurodegenerative and/or neuropsychiatric diseases. Lipkin and Hornig at the Center for Infection and Immunity have developed new tests to examine that pathway in people with chronic fatigue syndrome.
This is a whole new slant on ME/CFS.
The result is reduced serotonin uptake and increased serotonin levels in the synapses of the nerves. Serotonin has historically been associated with mood disorders but recent research indicates it impacts many areas of the body. We'll see in Darden's blog that serotonin has many immune effects. In fact, without adequate serotonin levels your immune system will not fight off an infection.
[fright]
The Mady Hornig and Ian Lipkin microbiome results are getting more interesting all the time. They believe that the substance serotonin is produced out of - tryptophan - may be being metabolized to kynurenine metabolites instead of serotonin. The kynurenine pathway has been associated with many neurodegenerative and/or neuropsychiatric diseases. Lipkin and Hornig at the Center for Infection and Immunity have developed new tests to examine that pathway in people with chronic fatigue syndrome.
This is a whole new slant on ME/CFS.
PLoS One. 2015 Oct 16;10(10):e0140883. doi: 10.1371/journal.pone.0140883. eCollection 2015.Maintenance of Chronic Fatigue Syndrome (CFS) in Young CFS Patients Is Associated with the 5-HTTLPR and SNP rs25531 A > G Genotype.
Meyer B1, Nguyen CB1, Moen A2, Fagermoen E3, Sulheim D4, Nilsen H5, Wyller VB6, Gjerstad J2.
Author information
Abstract
- 1Dept. of Paediatrics, Akershus University Hospital, Oslo, Norway.
- 2Dept. of Physical Medicine and Rehabilitation, Oslo University Hospital, Oslo, Norway; National Institute of Occupational Health, Oslo, Norway; Department of Biosciences, University of Oslo, Oslo, Norway.
- 3Dept. of Anaesthesiology and Critical Care, Oslo University Hospital, Oslo, Norway; Institute of Clinical Medicine, Medical Faculty, University of Oslo, Oslo, Norway.
- 4Dept. of Paediatrics, Lillehammer County Hospital, Lillehammer, Norway; Dept. of Paediatrics, Oslo University Hospital, Oslo, Norway.
- 5Institute of Clinical Medicine, Medical Faculty, University of Oslo, Oslo, Norway; Section for Clinical Molecular Biology, Akershus University Hospital, Oslo, Norway.
- 6Dept. of Paediatrics, Akershus University Hospital, Oslo, Norway; Institute of Clinical Medicine, Medical Faculty, University of Oslo, Oslo, Norway.
Earlier studies have shown that genetic variability in the SLC6A4 gene encoding the serotonin transporter (5-HTT) may be important for the re-uptake of serotonin (5-HT) in the central nervous system. In the present study we investigated how the 5-HTT genotype i.e. the short (S) versus long (L) 5-HTTLPR allele and the SNP rs25531 A > G affect the physical and psychosocial functioning in patients with chronic fatigue syndrome (CFS). All 120 patients were recruited from The Department of Paediatrics at Oslo University Hospital, Norway, a national referral center for young CFS patients (12-18 years). Main outcomes were number of steps per day obtained by an accelerometer and disability scored by the Functional Disability Inventory (FDI).
Patients with the 5-HTT SS or SLG genotype had a significantly lower number of steps per day than patients with the 5-HTT LALG, SLA or LALA genotype. Patients with the 5-HTT SS or SLG genotype also had a significantly higher FDI score than patients with the 5-HTT LALG, SLA or LALA genotype.
Thus, CFS patients with the 5-HTT SS or SLG genotype had worse 30 weeks outcome than CFS patients with the 5-HTT LALG, SLA or LALA genotype. The present study suggests that the 5-HTT genotype may be a factor that contributes to maintenance of CFS.
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